reticulocyte count and circulating nucleated red blood cells are usually elevated (Platt et al., 1994). 1.2.3.8. Acute chest syndrome (ACS) Acute chest syndrome is a life‐threatening condition for SCD patients. It is the second most frequent reason for hospitalization in children and adults with SCD and 11 the most common cause of death. It's similar to pneumonia and is caused by an infection or by sickle cells trapped in the lungs. Patients with this condition usually have chest pain, fever, and an abnormal chest x ray. Over time, lung damage may lead to pulmonary hypertension (Smith et al., 2000). 1.2.3.9. Acute stroke Stroke is one of the most common and devastating complications of SCD (OheneFrempong et al., 1998) Sickle‐shaped red blood cells may stick to the walls of the tiny blood vessels in the brain. This type of stroke occurs mainly in children. This complication presents as sudden onset of weakness, aphasia, and sometimes seizures or coma and results in adverse motor and cognitive squeal. In the absence of secondary prevention measures such as a chronic transfusion program or hematopoietic stem cell transplantation, recurrence rates have been shown to range between 46 and 90 percent in children with SCD. Brain hemorrhage occurs more often in adult’s patients (Verduzco and Nathan, 2005). 1.2.3.10. Priapism Males with sickle cell disease may have painful and unwanted erections lasting about 4 hours, called priapism. This happens because the sickle cells stop blood flow out of an erect penis. Priapism is a common complication of SCD, affecting 35 percent of male patients, over time, priapism can damage the penis and lead to impotence (Olujohungbe et al., 2011). 1.2.3.11. Multisystem organ failure Multisystem organ failure is a severe, rare and life-threatening complication usually associated with a VOC and characterized by failure of the lungs, liver, and/or kidneys. Symptoms linked to this complication are fever and changes in mental 12 status such as sudden tiredness and loss of interest in their surroundings. The incidence of chronic complications appears to increase with age and understanding of the pathophysiology and the involved factors is necessary to prevent or reduce long‐term morbidity (Hassell et al., 1994). 1.2.3.12. Avascular necrosis Avascular or aseptic necrosis can occur when capillaries are occluded by sickled erythrocytes at distal portions of a bone, near a joint, where hypoxia is maximal and collateral circulation is inadequate, the femoral neck is the most common site of aseptic necrosis. It causes chronic severe pain and disability (Diggs, 1967). 1.2.3.13. Leg ulcers Leg ulcers are a common complication of SCD. Sickle cell ulcers usually begin as small sores on the lower third of the leg. Leg ulcers occur more often in males than in females and usually appear between the ages of 10 and 50. The cause of leg ulcers is not clear. Some heal rapidly, but others persist for years or recur. (Mason, 1922). 1.2.3.14. Pulmonary Hypertension Pulmonary hypertension (PH) is defined as an elevation of the resting mean pulmonary arterial pressure (>25 mmHg) as determined by right heart catheterization (RHC). PH can occur in chronic hemolytic anemia and in the setting of chronic lung disease, chronic thromboembolic disease, or can be due to unclear and multiple mechanisms. Initial testing for PH has been done with an echocardiography assessment to estimate pulmonary artery pressure using tricuspid regurgitant jet velocity (TRV), but diagnosis requires right heart catheterization and direct measurement of the pulmonary arterial pressure and vaso-reactivity of the vessels. Excessive shortness of breath is an important symptom of PH (Badesch et al., 2009). 13 1.2.3.15. Ophthalmologic complications Chronic ophthalmological complications of SCD include proliferative sickle retinopathy and vitreous hemorrhage. They occur in up to 50 percent of patients with SCD and are associated with significant visual loss (Moriarty et al., 1988). The symptoms and complications of sickle cell disease (SCA) arise mainly from the crisis, activation and damage of endothelial cells with activation of adhesion molecules lead to inflammation, release of C-reactive protein (CRP) and other inflammatory mediators and subsequent enhancement of ischemia (Manwani and Frenette, 2013). The above and other lines of evidence suggest that SCD is associated with a chronic inflammatory state, in which inflammation, oxidative stress and tissue oxidative damage occur, leading to various degrees of disease severity and end-organ dysfunction. Exploring the role of CRP in this chronic inflammatory state is very important as we search for therapeutic targets in this disease. 1.2.4. The C-reactive protein The C-reactive protein (CRP) is an acute phase reactant, a protein made by the liver and released into the blood within a few hours after tissue injury, the start of an infection, or other cause of inflammation. Discovered in Oswald Avery's laboratory during the course of studies of patients with Streptococcus pneumonia infection( Tillet, and Francis, 1930) Sera obtained from these patients during the early, acute phase of the illness were found to contain a protein that could precipitate the “C” polysaccharide derived from the pneumococcal cell wall. Forty years later, Volakis and Kaplan identified the specific ligand for CRP in the pneumococcal C